中文摘要：

从转基因的鼠标， immunoprecipitation 数据，基因表达式分析，和功能的 heterologous 表达式研究的引人注目的证据支持了 Kv 隧道交往的角色蛋白质(KChIPs ) 作为位于心脏的短暂外面的水流和 neuronal A 类型电流下面的 Kv4 (Shal ) 隧道的调节的人。到现在为止，有四个成员(KChIP14 ) ，在这个家庭识别。KChIP1 在大脑主要被表示，与在小脑，网状的 thalamic 原子核，中间的 habenular 原子核，马头鱼尾的怪兽，和 striatum 的 Purkinje 房间的相对丰富。我们从在 situ 杂交和 immunostaining 试金的结果表明 KChIP1 在与 GABAergic 禁止的神经原建议它的功能的关系的 parvalbumin 积极的神经原的 subpopulation 被表示。而且，从 KChIP1 缺乏的鼠标获得的结果证明那个 KChIP1 变化没损害幸存或改变全面大脑体系结构，在大脑开发对它的必要函数争论。然而，适用的 KChIP1 删除显示出的老鼠增加了危险性到 anti-GABAergic 起痉挛的药导致 pentylenetetrazole 的抓住，显示那 KChIP1 可能在 GABAergic 禁止的系统起枢轴的作用。

英文摘要：

Compelling evidences from transgenic mice, immunoprecipitation data, gene expression analysis, and functional heterologous expression studies supported the role of Kv channel interacting proteins （KChIPs） as modulators of Kv4 （Shal） channels underlying the cardiac transient outward current and neuronal A-type current. Till now, there are four members （KChIP1-4） identified in this family. KChIP1 is expressed predominantly in brain, with relative abundance in Purkinje cells of cerebellum, the reticular thalamic nuclei, the medial habenular nuclei, the hippocampus, and striaturn. Our results from in situ hybridization and immunostaining assay revealed that KChIP1 was expressed in a subpopulation of parvalbumin-positive neurons suggesting its functional relationship with the GABAergic inhibitory neurons. Moreover, results obtained from KChIP1-deficient mice showed that KChIP1 mutation did not impair survival or alter the overall brain architecture, arguing against its essential function in brain development. However, the mice bearing KChIP1 deletion showed increased susceptibility to anti-GABAergic convulsive drug pentylenetetrazole-induced seizure, indicating that KChIP1 might play pivotal roles in the GABAergic inhibitory system.